VT_MONOMORPHIC
Technical documentation
Sustained Monomorphic Ventricular Tachycardia
≥ 3 consecutive ventricular complexes at a rate > 100 bpm with uniform QRS morphology. Usually caused by reentry around myocardial scar (post-infarction). Hallmarks include AV dissociation (independent P waves, fusion beats, capture beats) and extreme axis deviation.
Also known as: Sustained Monomorphic Ventricular Tachycardia · taquicardia ventricular · TV monomorfa · TV sostenida · TVMS · taquicardia ventricular monomorfa sostenida · monomorphic ventricular tachycardia · monomorphic VT · VT · MVT
What parameters does the model use?
The following values are applied by the simulation engine to this entity. They govern activation kinematics in the 3D model and the real-time synthesis of the 12-lead electrocardiogram.
What parameters does the model use?
| Parameter | Model value |
|---|---|
| Mechanism | Reentrada |
| Modeled rate | 120–200 bpm (default 160) |
| Regularity | Regular |
| P wave | Dissociated from QRS |
| QRS duration | 160 ms |
| QRS morphology | Wide, ventricular origin |
| AV conduction | Atrioventricular dissociation |
| Severity | Life-threatening |
Which leads should be evaluated?
The catalog marks as primary diagnostic leads V1, V6, aVR, II. Uniform wide QRS complexes; look for AV dissociation, capture beats, and fusion beats.
In the simulator, these leads are highlighted on the 12-channel tracing and corresponding vectors are rendered on the 3D model, displaying electrical changes and anatomical origin simultaneously.
Frequently asked clinical questions
How is Sustained Monomorphic Ventricular Tachycardia identified on the 12-lead ECG?
≥ 3 consecutive ventricular complexes at a rate > 100 bpm with uniform QRS morphology. Usually caused by reentry around myocardial scar (post-infarction). Hallmarks include AV dissociation (independent P waves, fusion beats, capture beats) and extreme axis deviation. The characteristic diagnostic waveforms are generated in real time across the simulated 12-lead tracing.
Which leads are critical for diagnostic confirmation?
The primary diagnostic leads are V1, V6, aVR, II. Uniform wide QRS complexes; look for AV dissociation, capture beats, and fusion beats. In the simulator, these channels highlight the correlation with anatomical vectors.
What is the underlying electrophysiological or anatomical mechanism?
It originates from altered conduction in the cardiac conduction system, mediated by reentrada.
How can this condition be explored in the 3D simulator?
MioAtlas offers direct deep-link reproducibility with preconfigured parameters, allowing full 3D cardiac rotation and lead vector inspection.
How do you open this configuration?
The simulator encodes its full state in the query string, providing a stable and reproducible URL:
https://mioatlas.com/simulador/en/?mode=conduction&arr=VT_MONOMORPHIC&add=1
Related entities
Other entities in the same category within the catalog:
Related clinical comparisons
Sources and bibliographic references
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Anderson RH, Yanni J, Boyett MR, Chandler NJ, Dobrzynski H (2009). "The anatomy of the cardiac conduction system". Clin Anat.
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Rautaharju PM, Surawicz B, Gettes LS, et al. (2009). "AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part IV: The ST segment, T and U waves, and the QT interval". Circulation.
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Kligfield P, Gettes LS, Bailey JJ, et al. (2007). "Recommendations for the standardization and interpretation of the electrocardiogram: Part I: The electrocardiogram and its technology". Circulation.